ArticleJournal of inflammation research2025
Inflammation-Induced Nitric Oxide Synthase May Mediate the Acute Hypotensive Effect of ST36 Stimulation.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Acupoint Zusanli (ST36) has been shown to reduce blood pressure, but the underlying mechanism remains unknown. This study aimed to characterize the effects of manual acupuncture (MA) at ST36 on BP and its associated mechanisms in anesthetized rats. Methods: The cardiovascular response to MA at ST36 in Sprague-Dawley rats was measured by electrocardiogram, hemodynamic methods, heart rate variability, echocardiography, laser speckle contrast imaging, and Western blotting. RNA sequencing was employed for mechanistic investigation, and validation was performed through blood enzyme-linked immunosorbent assay and pharmacologic inhibition. Results: Stimulation of ST36 increased peripheral blood flow while decreasing the velocity time integral of the femoral artery and cardiac stroke volume. This stimulation induced transient hypotension, accompanied by a decreased heart rate and reduced cardiac contractility, thereby exerting negative chronotropic and inotropic effects on the heart. Furthermore, the increased low-/high-frequency ratio after ST36 stimulation, along with the upregulation of phosphorylated tyrosine hydroxylase, indicated sympathetic activation. RNA sequencing at the local acupoint revealed enrichment of inflammation-related pathways following ST36 stimulation, which was corroborated by elevated tumor necrosis factor-alpha (TNF-α) levels in the serum. Notably, the nitric oxide synthase (NOS) inhibitor L-NG-Nitro arginine methyl ester (L-NAME) effectively suppressed the induced hypotension. Conclusion: These results indicated that MA at ST36 induced inflammation, which activated NOS and resulted in the release of nitric oxide. This led to the vasodilation of peripheral vessels and transient hypotension.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.